Inhibition of osteoblast differentiation by aluminum trichloride exposure is associated with inhibition of BMP-2/Smad pathway component expression.

Bone morphogenetic protein-2 (BMP-2)/Smad signaling pathway plays an important role in regulating osteoblast (OB) differentiation. OB differentiation is a key process of bone formation. Aluminum (Al) exposure inhibits bone formation and causes Al-induced bone disease. However, the mechanism is not fully understood. To investigate whether BMP-2/Smad signaling pathway is associated with OB differentiation in aluminum trichloride (AlCl)-treated OBs, the primary rat OBs were cultured and exposed to 0 (control group, CG), 1/40 IC (low-dose group, LG), 1/20 IC (mid-dose group, MG), and 1/10 IC (high-dose group, HG) of AlCl for 24 h, respectively. We found that the expressions of OB differentiation markers (Runx-2, Osterix and ALP) and BMP-2/Smad signaling pathway components (BMP-2, BMPR-IA, p-BMPR-IA, BMPR-II, p-Smad1/5/8 and p-Smad1/5/8/4) were all decreased in AlCl-treated OBs compared with the CG. These results indicated that inhibition of OB differentiation by AlCl was associated with inhibition of BMP-2/Smad pathway component expression. Our findings provide a novel insight into the mechanism of AlCl-induced bone disease.